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Multiple myeloma (MM) is a blood cancer characterized by excess plasma cells in the bone marrow, which produce an abnormally high amount of monoclonal proteins. Untreated, the accumulation of these proteins can lead to end-organ damage. Most multiple myeloma cases evolve from monoclonal gammopathy of undetermined significance (MGUS), a premalignant state in which abnormal monoclonal proteins are detected in the blood. Although significant progress has been made in recent years, MM remains incurable. Treatment regimens usually consist of chemotherapy, targeted therapy, immunotherapy, immunomodulatory drugs, and steroids. Normally, a combination of drugs is administered in order to elicit the best response. Patients eligible for transplant undergo induction therapy to rapidly reduce the number of multiple myeloma cells followed by autologous hematopoietic stem cell transplant (HSCT) to replenish blood cell counts. Other patients are treated with cancer drug combinations, such as daratumumab, lenalidomide, and dexamethasone. Daratumumab is a monoclonal antibody that targets proteins on MM cells, marking them for destruction by the immune system. Lenalidomide is an anti-angiogenic drug that prevents blood vessel growth. Dexamethasone is a corticosteroid that induces apoptosis in MM cells. In patients that undergo relapse, treatments such as bispecific monoclonal antibodies and CAR T-cell therapy have become more common. Patients who have certain disease characteristics, such as the presence of a t(4;14) or t(14;16) translocation, deletion of 17p, and amplification of chromosome 1, experience lower survival rates. There is a poor prognosis for these patients, creating a need for novel tailored therapeutic options. MM cells express certain markers on their surface that set them apart from healthy plasma cells, including CD56, which is present in a notable proportion of MM patients. Patients with significantly greater CD56 expression have inferior outcomes compared to their counterparts. We have previously demonstrated that CD56 (also known as neuronal cell adhesion molecule), a surface glycoprotein aberrantly expressed in more than seventy percent of patients with multiple myeloma (MM), promotes CREB1 phosphorylation and its binding to the DNA, leading to genomic transcription. CREB1 (cAMP responsive element binding protein 1) is a transcription factor involved in several aspects of MM cellular growth and metabolism. In previous studies, we have demonstrated that CREB1 inhibitors are toxic towards MM cells and activate natural killer cell immunity by decreasing HLA-E expression. However, we hypothesize that CREB1 could have other functions in MM. This study aims to characterize the role of CREB1 in modulating autophagy and the unfolded protein response, and its interactions with TXNIP in regulating oxidative stress.